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51/100

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Lewy body dementia

Topic: Brain proteins, microglia and lab models

Pathologic TAR-DNA-binding protein 43 (TDP-43) is a disease protein in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis. We studied the presence, frequency, and distribution of TDP-43 pathology by immunohistochemistry and biochemistry in a series of clinically well-characterized tauopathy patient brains, including 182 Alzheimer disease (AD), 39 corticobasal degeneration, 77 progressive supranuclear palsy, and 12 Pick disease cases and investigated the clinical impact of concomitant TDP-43 pathology in these cases. TAR-DNA-binding protein 43 pathology was found in 25.8% of AD cases. It was restricted to the dentate gyrus and entorhinal cortex in approximately 75% of cases; approximately 25% showed more widespread TDP-43 pathology in frontal and temporal cortices, resembling the FTLD-U subtype associated with progranulin mutations. TAR-DNA-binding protein 43 pathology in AD was associated with significantly longer disease duration, but there was no association with the clinical presentation (148 cases diagnosed as AD and 34 cases diagnosed as frontotemporal lobar degeneration). Progressive supranuclear palsy and Pick disease cases showed no TDP-43 inclusions and no biochemical alterations of TDP-43. There was, however, a unique, predominantly glial TDP-43 pathology with staining of astrocytic plaque-like structures and coiled bodies in 15.4% of corticobasal degeneration cases; this was associated with biochemical TDP-43 changes similar to those in FTLD-U. These findings provide further insight into the burden and clinical significance of TDP-43 pathology in disorders other than FTLD-U and amyotrophic lateral sclerosis.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Uryu, K., Nakashima-Yasuda, H., Forman, M. S., Kwong, L. K., Clark, C. M., Grossman, M., et al. (2008). Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e31817713b5

Vancouver

Uryu K, Nakashima-Yasuda H, Forman MS, Kwong LK, Clark CM, Grossman M, et al. Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies. Journal of neuropathology and experimental neurology. 2008. doi:10.1097/nen.0b013e31817713b5. PMID: 18520774.

BibTeX

@article{uryu2008-18520774,
  author  = {Uryu, K. and Nakashima-Yasuda, H. and Forman, M. S. and Kwong, L. K. and Clark, C. M. and Grossman, M. and Miller, B. L. and Kretzschmar, H. A. and others},
  title   = {{Concomitant TAR-DNA-binding protein 43 pathology is present in Alzheimer disease and corticobasal degeneration but not in other tauopathies}},
  journal = {Journal of neuropathology and experimental neurology},
  year    = {2008},
  doi     = {10.1097/nen.0b013e31817713b5},
  pmid    = {18520774},
  url     = {https://doi.org/10.1097/nen.0b013e31817713b5}
}

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Key findings

It was restricted to the dentate gyrus and entorhinal cortex in approximately 75% of cases; approximately 25% showed more widespread TDP-43 pathology in frontal and temporal cortices, resembling the FTLD-U subtype associated with progranulin mutations.
TAR-DNA-binding protein 43 pathology in AD was associated with significantly longer disease duration, but there was no association with the clinical presentation (148 cases diagnosed as AD and 34 cases diagnosed as frontotemporal lobar degeneration).
There was, however, a unique, predominantly glial TDP-43 pathology with staining of astrocytic plaque-like structures and coiled bodies in 15.4% of corticobasal degeneration cases; this was associated with biochemical TDP-43 changes similar to those in FTLD-U.
These findings provide further insight into the burden and clinical significance of TDP-43 pathology in disorders other than FTLD-U and amyotrophic lateral sclerosis.

Why it matters

This study found that TDP-43 pathology was present in about 26% of Alzheimer's disease cases and was linked to longer disease duration, but not to how the disease presented clinically. It does not test any treatment or prevention, so it has no direct implications for treating, curing, or preventing Alzheimer's disease.

Study details

Effect size25.8%; 15.4%
Evidence strengthLow

How this study scored 51/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, studied in people and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology)
Journal's citation record	2 / 4	Journal of Neuropathology & Experimental Neurology: journal h-index 239 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2008 — within 20 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	2 / 3	Effect reported as a number, without an interval or test
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 386 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	19.3 citations a year over 20 year(s) since 2008
Impact for its field and year	4 / 6	Cited 18.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	4 / 6	Cited by 33 other studies in this library
Still being cited	2 / 4	Cited 40 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Manuela Neumann: h-index 90 (OpenAlex, whole career)
Institution's track record	2 / 3	University of California, San Francisco: institution h-index 1,915 (OpenAlex)
Multi-centre collaboration	2 / 3	OpenAlex lists 5 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 18520774)
Free to read	0 / 2	Behind a paywall — scores zero
Total	51 / 100	—

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